Reservoir/excess pressure

The reservoir-wave hypothesis grew out of our work on wave intensity analysis. It is, however, an independent idea and so it seemed reasonable to give it its own web site. There will be many cross-links between the two sites, but it should be possible to follow the discussion in these pages without reference to wave intensity analysis.

What are the reservoir and excess pressures?

The reservoir-wave hypothesis says that the measured pressure in an artery (or vein) can usefully be thought of as the sum of a reservoir pressure that is related to the global compliance and resistance of the arterial system and an excess pressure that depends on local conditions.

P = Preservoir + Pexcess



Separation of the pressure waveform in the radial artery into reservoir and excess pressures

The 'can' part of the definition is trivial; we can divide the measured pressure in any way that we want. More difficult is the 'useful' part of the hypothesis; demonstrating that the separation is useful is the goal of ongoing research and will be the major part of these pages.

Very recently (unpublished) we have suggested a new definition for the reservoir, and hence the excess, pressure that avoids some of the conceptual difficulties with our original definition. More importantly, we have also shown that this reservoir pressure represents the minimum hydraulic work that the ventricle must do to provide a given flow waveform with the given net arterial compliance and resistance. This is very interesting because it provides a reasonable physical explanation for some of the recent clinical observations arising from the separation of the pressure waveform into reservoir and excess pressures.

The clinical results are also very new (unpublished). The details of the study are elsewhere in these pages (Cafe study) but briefly it is found that the integral of the excess pressure over the cardiac period is the 'best' indicator of cardiac events (heart attack or stroke). In addition to explaining the difference in outcomes for the two pharmacological interventions (amlodipine and atenolol), separation of the study population into two cohorts based on the median excess pressure integral produced a highly significant difference in clinical outcomes.

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Latest update: 08 October 2010